bims-agimec Biomed News
on Aging mechanisms
Issue of 2024–11–03
seven papers selected by
Metin Sökmen, Ankara Üniversitesi
  1. Aging Skeletal Muscles: What Are the Mechanisms of Age-Related Loss of Strength and Muscle Mass, and Can We Impede Its Development and Progression?
  2. Sex as a biological variable in ageing: insights and perspectives on the molecular and cellular hallmarks.
  3. The evolution of ageing: classic theories and emerging ideas.
  4. Five-factor theory of aging and death due to aging.
  5. The immunometabolic roots of aging.
  6. The 3 I's of immunity and aging: immunosenescence, inflammaging, and immune resilience.
  7. The Role of Non-Coding RNAs in Mitochondrial Dysfunction of Alzheimer's Disease.
  1. Int J Mol Sci. 2024 Oct 11. pii: 10932. [Epub ahead of print]25(20):
    Aging Skeletal Muscles: What Are the Mechanisms of Age-Related Loss of Strength and Muscle Mass, and Can We Impede Its Development and Progression?
    Thomas Gustafsson, Brun Ulfhake.
      As we age, we lose muscle strength and power, a condition commonly referred to as sarcopenia (ICD-10-CM code (M62.84)). The prevalence of sarcopenia is about 5-10% of the elderly population, resulting in varying degrees of disability. In this review we emphasise that sarcopenia does not occur suddenly. It is an aging-induced deterioration that occurs over time and is only recognised as a disease when it manifests clinically in the 6th-7th decade of life. Evidence from animal studies, elite athletes and longitudinal population studies all confirms that the underlying process has been ongoing for decades once sarcopenia has manifested. We present hypotheses about the mechanism(s) underlying this process and their supporting evidence. We briefly review various proposals to impede sarcopenia, including cell therapy, reducing senescent cells and their secretome, utilising targets revealed by the skeletal muscle secretome, and muscle innervation. We conclude that although there are potential candidates and ongoing preclinical and clinical trials with drug treatments, the only evidence-based intervention today for humans is exercise. We present different exercise programmes and discuss to what extent the interindividual susceptibility to developing sarcopenia is due to our genetic predisposition or lifestyle factors.
    Keywords:  ageing; dynapenia; motor unit; muscle fibre atrophy; senescence
    DOI:  https://doi.org/10.3390/ijms252010932
  2. Open Biol. 2024 Oct;14(10): 240177
    Sex as a biological variable in ageing: insights and perspectives on the molecular and cellular hallmarks.
    José Héctor Gibrán Fritz García, Claudia Isabelle Keller Valsecchi, M Felicia Basilicata.
      Sex-specific differences in lifespan and ageing are observed in various species. In humans, women generally live longer but are frailer and suffer from different age-related diseases compared to men. The hallmarks of ageing, such as genomic instability, telomere attrition or loss of proteostasis, exhibit sex-specific patterns. Sex chromosomes and sex hormones, as well as the epigenetic regulation of the inactive X chromosome, have been shown to affect lifespan and age-related diseases. Here we review the current knowledge on the biological basis of sex-biased ageing. While our review is focused on humans, we also discuss examples of model organisms such as the mouse, fruit fly or the killifish. Understanding these molecular differences is crucial as the elderly population is expected to double worldwide by 2050, making sex-specific approaches in the diagnosis, treatment, therapeutic development and prevention of age-related diseases a pressing need.
    Keywords:  X chromosome; X-chromosome inactivation; ageing; hallmarks of ageing; sex chromosomes; sex hormones
    DOI:  https://doi.org/10.1098/rsob.240177
  3. Biogerontology. 2024 Oct 29. 26(1): 6
    The evolution of ageing: classic theories and emerging ideas.
    Mark T Mc Auley.
      Ageing is generally regarded as a non-adaptive by-product of evolution. Based on this premise three classic evolutionary theories of ageing have been proposed. These theories have dominated the literature for several decades. Despite their individual nuances, the common thread which unites them is that they posit that ageing results from a decline in the intensity of natural selection with chronological age. Empirical evidence has been identified which supports each theory. However, a consensus remains to be fully established as to which theory best accounts for the evolution of ageing. A consequence of this uncertainty are counter arguments which advocate for alternative theoretical frameworks, such as those which propose an adaptive origin for ageing, senescence, or death. Given this backdrop, this review has several aims. Firstly, to briefly discuss the classic evolutionary theories. Secondly, to evaluate how evolutionary forces beyond a monotonic decrease in natural selection can affect the evolution of ageing. Thirdly, to examine alternatives to the classic theories. Finally, to introduce a pluralistic interpretation of the evolution of ageing. The basis of this pluralistic theoretical framework is the recognition that certain evolutionary ideas will be more appropriate depending on the organism, its ecological context, and its life history.
    Keywords:  Ageing; Evolution; Longevity; Pluralism; Senescence
    DOI:  https://doi.org/10.1007/s10522-024-10143-5
  4. Arch Gerontol Geriatr. 2024 Oct 19. pii: S0167-4943(24)00341-8. [Epub ahead of print]129 105665
    Five-factor theory of aging and death due to aging.
    Danko Obradovic.
      This new theory of aging explains that aging and death due to aging are due to five factors, and also explains how these factors are interconnected and jointly lead to aging and death of the organism, pointing to many facts that strongly support it. The first factor is the harmful changes that occur in cellular structures. The second factor is the cessation of cell division in adult organisms, which leads to the inability to restore cellular structures. The third factor is the feature that cells do not die due to the accumulation of harmful changes that occur in the cells during the life of the organism. The fourth factor is the inability of stem cells to regenerate tissue by replacing such cells with new ones, because somatic cells do not die and there are no signals that stimulate the proliferation of stem cells and their differentiation into new ones that would replace dead cells. The fifth factor is that all cells die suddenly, due to the cessation of one of the vital functions of the organism, and not gradually during life, due to a decrease in the functionality of cells caused by the introduction of harmful changes in cellular structures, which would allow stem cells to regenerate tissues and keep the body young. Also, to show that this aging theory is valid, the theory gives its view of the evolution of five factors, which according to this theory lead to aging, which gives strong support to this theory.
    Keywords:  Ageing; Aging; Evolution; Immortality; Regeneration
    DOI:  https://doi.org/10.1016/j.archger.2024.105665
  5. Curr Opin Immunol. 2024 Oct 25. pii: S0952-7915(24)00088-8. [Epub ahead of print]91 102498
    The immunometabolic roots of aging.
    Pierpaolo Ginefra, Helen C Hope, Girieca Lorusso, Patrizia D'Amelio, Nicola Vannini.
      Aging is one of the greatest risk factors for several chronic diseases and is accompanied by a progressive decline of cellular and organ function. Recent studies have highlighted the changes in metabolism as one of the main drivers of organism dysfunctions during aging and how that strongly deteriorate immune cell performance and function. Indeed, a dysfunctional immune system has been shown to have a pleiotropic impact on the organism, accelerating the overall aging process of an individual. Intrinsic and extrinsic factors are responsible for such metabolic alterations. Understanding the contribution, regulation, and connection of these different factors is fundamental to comprehend the process of aging and develop approaches to mitigate age-related immune decline. Here, we describe metabolic perturbations occurring at cellular and systemic levels. Particularly, we emphasize the interplay between metabolism and immunosenescence and describe novel interventions to protect immune function and promote health span.
    DOI:  https://doi.org/10.1016/j.coi.2024.102498
  6. Front Aging. 2024 ;5 1490302
    The 3 I's of immunity and aging: immunosenescence, inflammaging, and immune resilience.
    Marianna V Wrona, Rituparna Ghosh, Kaitlyn Coll, Connor Chun, Matthew J Yousefzadeh.
      As we age, our immune system's ability to effectively respond to pathogens declines, a phenomenon known as immunosenescence. This age-related deterioration affects both innate and adaptive immunity, compromising immune function and leading to chronic inflammation that accelerates aging. Immunosenescence is characterized by alterations in immune cell populations and impaired functionality, resulting in increased susceptibility to infections, diminished vaccine efficacy, and higher prevalence of age-related diseases. Chronic low-grade inflammation further exacerbates these issues, contributing to a decline in overall health and resilience. This review delves into the characteristics of immunosenescence and examines the various intrinsic and extrinsic factors contributing to immune aging and how the hallmarks of aging and cell fates can play a crucial role in this process. Additionally, it discusses the impact of sex, age, social determinants, and gut microbiota health on immune aging, illustrating the complex interplay of these factors in altering immune function. Furthermore, the concept of immune resilience is explored, focusing on the metrics for assessing immune health and identifying strategies to enhance immune function. These strategies include lifestyle interventions such as diet, regular physical activity, stress management, and the use of gerotherapeutics and other approaches. Understanding and mitigating the effects of immunosenescence are crucial for developing interventions that support robust immune responses in aged individuals.
    Keywords:  cellular senescence; immune resilience; immunosenescence; inflammaging; inflammation
    DOI:  https://doi.org/10.3389/fragi.2024.1490302
  7. J Mol Neurosci. 2024 Oct 28. 74(4): 100
    The Role of Non-Coding RNAs in Mitochondrial Dysfunction of Alzheimer's Disease.
    Samin Abed, Amir Ebrahimi, Fatemeh Fattahi, Ghazal Kouchakali, Mahmoud Shekari-Khaniani, Sima Mansoori-Derakhshan.
      Although brain amyloid-β (Aβ) peptide buildup is the main cause of Alzheimer's disease (AD), mitochondrial abnormalities can also contribute to the illness's development, as either a primary or secondary factor, as programmed cell death and efficient energy generation depend on the proper operation of mitochondria. As a result, non-coding RNAs (ncRNAs) may play a crucial role in ensuring that nuclear genes related to mitochondria and mitochondrial genes function normally. Interestingly, a significant number of recent studies have focused on the impact of ncRNAs on the expression of nucleus and mitochondrial genes. Additionally, researchers have proposed some intriguing therapeutic approaches to treat and reduce the severity of AD by adjusting the levels of these ncRNAs. The goal of this work was to consolidate the existing knowledge in this field of study by systematically investigating ncRNAs, with a particular emphasis on microRNAs (miRNAs), long non-coding RNAs (lncRNAs), circular RNAs (circRNAs), and small nucleolar RNAs (snoRNAs). Therefore, the impact and processes by which ncRNAs govern mitochondrial activity in the onset and progression of AD are thoroughly reviewed in this article. Collectively, the effects of ncRNAs on physiological and molecular mechanisms associated with mitochondrial abnormalities that exacerbate AD are thoroughly reviewed in the current research, while also emphasizing the relationship between disturbed mitophagy in AD and ncRNAs.
    Keywords:  Alzheimer’s disease; Mitochondrial dysfunction; Mitophagy; Non-coding RNAs
    DOI:  https://doi.org/10.1007/s12031-024-02262-y
This page is being maintained by Thomas Krichel. It was last updated on 2024‒11‒22 at 4:10.